ERDR1 enhances human NK cell cytotoxicity through an actin-regulated degranulation-dependent pathway
- Authors
- Lee, Ha-Reum; Huh, Scarlett Yoona; Hur, Dae Young; Jeong, Hyuk; Kim, Tae Sung; Kim, Sang Yoon; Park, Seung Beom; Yang, Yoolhee; Bang, Sa Ik; Park, Hyunjeong; Cho, Daeho
- Issue Date
- Nov-2014
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Natural killer cell; Erythroid differentiation regulator 1; Cytotoxicity; Immune system; Actin
- Citation
- CELLULAR IMMUNOLOGY, v.292, no.1-2, pp 78 - 84
- Pages
- 7
- Journal Title
- CELLULAR IMMUNOLOGY
- Volume
- 292
- Number
- 1-2
- Start Page
- 78
- End Page
- 84
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10766
- DOI
- 10.1016/j.cellimm.2014.10.002
- ISSN
- 0008-8749
1090-2163
- Abstract
- Erythroid differentiation regulator 1 (ERDR1), which is a stress-related survival factor, exhibits anticancer effects against melanoma. However, the function of ERDR1 on immune cells has not been examined. We investigated whether ERDR1 regulates the cytotoxic ability of human natural killer (NK) cells, which are known as innate effector lymphocytes. In this study, treatment with recombinant ERDR1 resulted in enhanced NK cell cytotoxicity through the secretion of lytic granules. Furthermore, actin modulation was involved in the ERDR1-enhanced NK cell cytotoxicity. ERDR1 stimulated actin accumulation at the immunological synapse, which was induced by the activation of Vav-1 in NK cells. These findings suggest new insight into the function of ERDR1 function in the human immune system. (C) 2014 Elsevier Inc. All rights reserved.
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